Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
Department of Cardiology, University of Pavia and IRCCS Policlinico S. Matteo, Pavia, Italy; 2University of
Virginia, Charlottesville, VA, U.S.A.; 3The Childrens Heart Program of South Carolina, Medical University of
South Carolina, Charleston, SC, U.S.A.; 4Pediatric Arrhythmias Center, IRCCS Istituto Auxologico Italiano,
Milan, Italy; 5Division of Pediatric Cardiology, Department of Pediatrics, Childrens Hospital of Philadelphia,
University of Pennsylvania School of Medicine, Philadelphia, PA, U.S.A.; 6Division of Pediatric Cardiology,
Department of Pediatrics, Hopital Necker Enfants Malades, Paris, France; 7Department of Paediatric Cardiology,
Freeman Hospital, Newcastle upon Tyne, U.K.
Introduction.............................................................1329
Normal electrocardiogram in the newborn .............1330
Normal values......................................................1330
Technology ..........................................................1330
Artefacts...............................................................1332
Electrocardiographic measurements ....................1332
Heart rate.............................................................1332
P wave..................................................................1332
QRS complex.......................................................1332
QT interval ..........................................................1333
ST segment and T wave ......................................1333
Abnormal electrocardiogram in the newborn .........1333
Heart rate.............................................................1333
Sinus arrhythmia..............................................1333
Sinus tachycardia .............................................1333
Sinus bradycardia.............................................1335
Other bradycardias...........................................1335
P wave..................................................................1335
Atrioventricular conduction.................................1335
Complete (3rd) atrioventricular block .............1335
1st and 2nd atrioventricular block...................1336
Intraventricular conduction .................................1336
Bundle branch block ........................................1336
Non-specific intraventricular conduction
abnormalities....................................................1336
WolParkinsonWhite syndrome ..................1336
QRS axis and amplitude......................................1338
Right ventricular hypertrophy .........................1338
Introduction
Most cardiologists who care for adults have no
or minimal experience with electrocardiograms
(ECGs) recorded in infants. So far, this has had no
practical implications because only seldom are they
requested to examine a neonatal ECG. This situation,
however, may change as some European countries
have begun to consider the possibility of introducing in their National Health Services the performance
of an ECG during the first month of life in all
newborns, as part of a cardiovascular screening
programme.
2002 Published by Elsevier Science Ltd on behalf of The European Society of Cardiology
1330
Technology
The normal newborn ECG should include 12 leads.
Other leads, V3R, V4R and V7, may provide additional
information to evaluate possible congenital heart
lesions.
The current use of computerized digital ECG systems
aects newborn ECGs to a greater extent than those of
older children or adults[7]. The newborn ECG may have
93154 (123)
91159 (123)
90166 (129)
107182 (149)
121179 (150)
01 days
13 days
37 days
730 days
13 months
+59
+64
+77
+65
+31
to
to
to
to
to
+192 (135)
+197 (134)
+187 (132)
+160 (110)
+114 (75)
Frontal plane
QRS axisa
(degrees)
Heart rate
(beats . min 1)
Age group
Table 1
28
28
29
30
26
P wave
amplitude
(mm)
008016 (011)
008014 (011)
008014 (010)
007014 (010)
007013 (010)
P-R
intervala
(s)
002008 (005)
002007 (005)
002007 (005)
002008 (005)
002008 (005)
QRS
durationa
V5
52
52
48
56
54
17
21
28
28
27
Q IIIc QV6c
(mm) (mm)
526
527
324
3215
3185
RV1b
(mm)
0225
021
017
011
0125
SV1b
(mm)
98
6
97
7
74
R/S V1c
011
012
0512
2516
521
RV6b
(mm)
098
095
098
098
072
10
11
10
12
12
28
29
25
22
29
52
52
48
47
53
SV6b
SV1 +RV6c R+SV4c
R/S V6c
(mm)
(mm)
(mm)
1332
Artefacts
Artefacts are common in newborn ECGs and include
limb lead reversal and incorrect chest lead positioning.
In addition, electrical interference, usually 60 cycles,
can occur in hospital settings from bedside monitors,
warmers or other equipment.
Other artefacts occur because of various types of
patient movement common in neonates. These artefacts
may be random as with hiccoughs or limb movement.
Normal complexes are seen along with the artefacts, and
the intrinsic rhythm of the patient is not aected. Other
common artefacts include a fine, often irregular undulation of the baseline from muscle tremors or jitteriness.
Again, the intrinsic rhythm is not aected. The size of
the QRS complex and the baseline may wander in a
cyclic fashion with respirations. It should be noted that
the neonate breathes from 3060 times per min.
The main clue in determining the presence of an
artefact is to evaluate whether it aects the intrinsic
rhythm and if it is timed such that it could be a true
depolarization. A signal within 80 ms from a true QRS
complex could not occur from an electrophysiologic
point of view.
Electrocardiographic measurements
Because of the current limitations of electronic measurements in newborn ECGs, intervals should be hand
measured as the computerized systems are often inaccurate in the newborn. Intervals in children increase with
increasing age, reaching most of the adult normal values
by 78 years of age.
Heart rate
Heart rate can be determined by a variety of methods. It
should be noted that normal neonates may have rates
Eur Heart J, Vol. 23, issue 17, September 2002
P wave
The P wave axis is a vector indicating the direction of
activation, which is away from the site of origin. By
identifying the quadrant location of the P wave axis one
can determine the site of origin of the rhythm. For
example, sinus rhythm originates in the high right
atrium transcribing a P wave with an axis in the quadrant bordered by 0 and +90. Measurements are available for P wave amplitude (Table 1). The P wave is
generally pointed in lead II and aVF and more rounded
in other leads. Lead V1 may be diphasic.
The PR interval is measured from the onset of the P
wave to the Q or R wave if no Q wave is present. The PR
interval, measured in lead II, increases with age and
decreases with heart rate. The normal neonatal PR
interval ranges from a minimum of 70 ms to a maximum
of 140 ms, with a mean of 100 ms.
QRS complex
The normal full-term neonate has an axis between 55
and 200 but by 1 month, the normal upper limit has
fallen to 160 or less. Although one might identify an
axis of 120 as right axis deviation in an adult, it is a
normal finding in a newborn. The QRS axis in the
premature newborn ECG ranges between 65 and 174.
The duration of the QRS complex is measured from
the beginning to the end of the ventricular depolarization complex and it should be measured in a lead with
an initial Q wave[5]. QRS duration in the newborn and
infant is narrow (<80 ms). Normal QRS duration increases with age. Normal values for QRS complex
duration in lead V5 are displayed in Table 1.
QRS morphology in the newborn may have more
notches and direction changes than seen in older children or adults. The direction of the Q wave in the
precordial or horizontal plane indicates the direction of
septal depolarization. Normally, there is a Q wave in
leads V5V6 indicating depolarization from left to right.
Normal values of Q wave amplitudes vary with the lead
and with age. Q wave amplitudes may be as high
1333
QT interval
The QT interval is the interval between the beginning of
the QRS complex and the end of the T wave. The QT
measurement should be made in leads II, V5, and V6
with the longest value being used. The main diculty lies
in identifying correctly the point where the descending
limb of the T wave intersects the isoelectric line. Due to
the fast heart rate of infants the P wave may be
superimposed on the T wave, particularly when the QT
interval is prolonged. In this case, the end of the T wave
should be extrapolated by drawing a tangent to the
downslope of the T wave and considering its intersection
with the isoelectric line.
The QT interval duration changes with rate and it is
usually corrected (QTc) by using Bazetts formula. Correction of the QT interval requires a stable sinus rhythm
without sudden changes in the RR interval. QTc is equal
to QT interval in seconds divided by the square root of
the preceding RR interval in seconds. To avoid timeconsuming calculations, a simple chart (Fig. 1) where
the value of QTc is easily obtained by matching QT and
RR interval in millimetres (given the paper speed at
25 mm . s 1) has been produced. When heart rate is
particularly slow or fast the Bazetts formula may not be
accurate in the correction but it remains the standard for
clinical use.
The mean QTc on the 4th day of life is 40020 ms[1]
and, at variance with the adult, no gender dierences are
present[14]. Therefore, the upper normal limit of QTc (2
standard deviations above the mean, corresponding to
the 975 percentile) is 440 ms. By definition, 25% of
normal newborns are expected to have a QTc greater
than 440 ms. In healthy infants there is a physiological
prolongation of QTc by the second month (mean
410 ms) followed by a progressive decline[15], so that by
the sixth month QTc returns to the values recorded in
the first week.
Pitfalls with QT measurement. Despite its apparent
simplicity the measurement of the QT interval is fraught
with errors. The simple fact that a small square on the
ECG paper is equivalent to 40 ms explains why healthy
scepticism should accompany claims of clinical importance attached to very small degrees of QT prolongation. An attempt should be made to measure with
Figure 1 Chart for calculation of QTc. QTc, according to the Bazetts formula is obtained by matching QT and RR interval in millimetres, given the paper speed
at 25 mm . s 1. Corresponding values of RR interval and uncorrected QT interval are also indicated.
1334
Task Force Report
1335
P wave
Abnormal P waves may be seen in infants with atrial
enlargement or non-sinus origin of the P wave. Ectopic
atrial rhythms originate most commonly from the low
right atrium (0 to 90), high left atrium (+90 to
+180) or the low left atrium (+180 to +270).
Right atrial enlargement and/or hypertrophy typically
produces increased P wave amplitude with a normal P
wave duration. The P wave axis usually remains normal
so the eect is usually best seen in lead II.
Left atrial enlargement and/or hypertrophy typically
produces an increased and prolonged negative terminal
deflection of the P wave in lead V1 (generally accepted as
>40 ms in duration and 01 mV in amplitude). Left atrial
enlargement also causes exaggerated notching of the P
wave in lead II although this is not a specific sign.
Work-up
An echocardiogram should be performed when clinically
indicated.
Atrioventricular conduction
During atrial tachycardia, it is possible to observe 1/1
conduction through the atrio-ventricular node at rates
over 300 beats . min 1.
Complete (third degree) atrioventricular block
Complete AV block implies complete absence of conduction from atrium to ventricle. ECG shows normal
atrial activation and slower dissociated regular QRS
complexes. Congenital complete block is observed in
complex congenital heart malformations[18].
Approximately one out of every 15 000 to 20 000 live
births results in a baby with isolated AV block. The
association between isolated neonatal AV block and
maternal connective tissue disease is well established and
ascribed to the presence of anti Ro/SSA and La-SSB
antibodies in the mothers. Nearly every mother with an
aected child has circulating antibodies. However, only
2 to 5% of women with known antibodies will have a
Eur Heart J, Vol. 23, issue 17, September 2002
1336
Intraventricular conduction
Bundle branch block
Congenital isolated complete right (RBBB) and left
bundle branch block are very rare in neonates. Southall
et al. found only one case of complete RBBB in a
population of 3383 apparently healthy newborn infants[27]. The classical ECG in Ebsteins anomaly of the
tricuspid valve displays a prolonged PR interval and a
wide RBBB. Left anterior fascicular block is found in
association with congenital heart malformations such as
atrio-ventricular canal defects and tricuspid atresia. In
severe cardiomyopathy, interruption of the left bundle,
which results from the involvement of the left ventricle
and/or its conduction system, has been reported and
carries a poor prognosis[28].
Eur Heart J, Vol. 23, issue 17, September 2002
Figure 2
ECG in a neonate showing subtle signs of WPW. Note delta waves in V5 and V6 with absence of Q waves.
1338
l-transposition of the great arteries, hypertrophic cardiomyopathy and cardiac tumours are associated with an
increased prevalence of preexcitation[36,37].
Clinical counterparts. In WPW syndrome the typical
form of paroxysmal supraventricular tachycardia (orthodromic) results from reentry antegradely through the
atrioventricular node and retrogradely through the accessory pathway. As digoxin shortens the antegrade
eective refractory period of the accessory pathway and
promotes rapid atrioventricular conduction during atrial
flutter or atrial fibrillation over the pathway, the use of
digoxin is contraindicated at any age [38,39]. Verapamil
should also be avoided as it may increase the ventricular
response rate during atrial fibrillation in those patients,
and may cause cardiovascular collapse in infants and
young children.
The incidence of sudden death in preexcitation syndrome during childhood has been estimated to be as
high as 05%[34] and cardiac arrest may be the initial
presentation in children with preexcitation[35]. However,
data on newborns and infants are lacking. One study on
a series of 90 newborns and infants with WPW syndrome and supraventricular tachycardia reported sudden death in two patients with a normal heart during
follow-up. Both infants, however, had been treated with
digoxin[36].
Finally, there are no sucient data on newborns and
infants with an incidental finding of preexcitation on
ECG concerning the occurrence of paroxysmal supraventricular tachycardia later on during their life.
Work-up
Congenital heart disease is more common in infants and
young children with preexcitation, with a prevalence as
high as 45% for infants with an ECG pattern consistent
with a right-sided accessory pathway[36]. Thus, in every
young patient with a preexcitation pattern on surface
ECG, a complete 2-dimensional echocardiographic
work-up is recommended to rule out any intracardiac
abnormality.
Assessment of the conduction properties of the accessory pathway, i.e. the antegrade eective refractory period
and the shortest RR-interval with preexcitation, by transesophageal programmed stimulation may be useful in
selected patients for risk stratification and mode of
therapy.
Ventricular repolarization
There is a simple reason that makes clinically important
the analysis of ventricular repolarization abnormalities:
their presence could be the harbinger of a significant risk
for life-threatening arrhythmia. It is established that
newborns found to have a prolonged QTc (>440 ms) on
the fourth day of life have an increased risk for sudden
death[1]. Some of these sudden deaths have previously
been labelled as Sudden Infant Death Syndrome.
On the other hand, the presence of confounding
factors above all the ambiguities in their
quantification calls for caution before making hasty
diagnoses associated with need for therapy and with
considerable parental anxiety.
Ventricular repolarization can be evaluated on the
surface ECG by measuring the QT interval duration and
by analysing the morphology of the ST segment and of
the T wave. Measurements of the QT interval should be
performed by hand.
It is important to remember that QT duration may
change over time. Accordingly, it is recommended
1339
Figure 3 ECG tracings of three newborns with LQTS diagnosed in the first months of life. Mutations on the
potassium channel gene KvLQT1 (panel A) and on the sodium channel gene SCN5A (panel B) were identified. Panel
B modified from ref. [44].
1340
Figure 4 QT prolongation management flow chart. Electrolytes, echocardiogram, intracranial ultrasound are recommended in the appropriate clinical situation. In cases of positive genetics and QTc >440 ms, therapy is indicated. #In
cases of a positive family history (Hx) for LQTS; *See text.
have additional importance. The following stepwise approach involves infants with and without a family history
for LQTS (Fig. 4). If family history is positive, then as
LQTS is an autosomal dominant disease the infant has
a 50% probability of being aected and complete diagnostic procedures should be performed, as always with LQTS
families.
The second ECG is normal.
If the first QTc was <470 ms, dismiss the case. If the
first QTc was d470 ms, then plan a third ECG after
12 months to remain on the safe side.
The second ECG shows a QTc between 440 and 470 ms.
In these cases with persistent borderline QT prolongation,
electrolytes, including calcium and magnesium, should be
checked. Clinical history of autoimmune disease and
plasma titres of maternal antibodies (anti Ro/SSA and
antiLa) should be performed. T wave morphology may be
helpful; for example, the presence of notches on the T
wave in the precordial leads further suggests the presence
of LQTS[48]. Additionally, mild bradycardia can also be
found in LQTS. ECGs should be obtained from the
parents and siblings of the neonate.
In the absence of family history of LQTS, symptoms
or arrhythmias, a 24-h Holter monitoring should be
obtained to look for T wave alternans, complex ventricular arrhythmias or marked QTc prolongation, and the
ECG should be periodically checked during the first
year. No treatment is currently recommended. With a
positive family history, the probability of LQTS becomes
high. Additional diagnostic procedures (24-h Holter
monitoring, echocardiogram and genetic screening)
should be performed and initiation of therapy could be
considered.
The second ECG shows a QTc d470 and <500 ms.
All diagnostic procedures listed above should be performed
and a third ECG should be planned within a month. In
case of a positive family history, therapy should be
initiated. Even without a family history, therapy should be
considered.
Even in infants with a very prolonged QTc in the first
month of life, the ECG may normalize. If subsequent
1341
Figure 5 ECG tracings of a newborn with blocked atrial bigeminy which simulates sinus bradycardia. Blocked
P waves are present when examining the T waves.
ECGs and diagnostic procedures do not confirm the
presence of LQTS, it is logical to progressively withdraw
therapy and to return to periodic observations.
The second ECG shows a QTc d500 ms.
Infants with a QTc d500 ms are very likely to be aected
by LQTS and to become symptomatic. All diagnostic
procedures listed above should be performed and these
infants should be treated.
Highest risk. The presence of QTc close to 600 ms, or of
T wave alternans, or of 2:1 AV block secondary to major
QT prolongation, or of hearing loss, identify infants at
extremely high risk[47,49].
ST segment elevation
Causes. There are multiple causes of ST segment elevation in infancy. The most frequent is pericarditis. Less
frequent causes of ST segment elevation with or without
T wave abnormalities are hyperkalaemia, intracranial
haemorrhage, pneumothorax and pneumopericardium,
subepicardial injury due to anomalous left coronary
artery or to Kawasaki disease with cardiac involvement.
Whenever an anomalous left coronary artery or, more
frequently, Kawasaki disease produce an acute myocardial infarction, QT prolongation may also be present.
ST segment elevation with a RBBB pattern in the
right precordial leads (V1V2) is the typical finding of the
Brugada syndrome, a genetic disorder associated with a
high incidence of sudden cardiac death secondary to
ventricular fibrillation, in the absence of cardiac structural abnormalities[50]. The ST segment elevation is
typically downsloping or coved and it is followed by a
negative T wave, at variance with the early repolariz-
1342
Table 2
SVT
Atrial flutter
VT
History
Rate
200500 b/min
R-R interval
variation
P wave axis
QRS
SVT=Supraventricular tachycardia.
VT=ventricular tachycardia.
1343
Conclusion
The main objective of the present document was to
provide cardiologists, who work with adults, with a
practical approach to neonatal electrocardiography, and
paediatricians and neonatologists with a tool that should
facilitate medical interaction on cardiologic issues. There
are important dierences between neonatal and adult
ECGs. When a cardiologist examines the ECG of an
apparently normal and healthy infant the focus has to be
on distinguishing between patterns that should cause no
alarm and those that require action or additional investigations. To provide clues for this distinction is what the
members of the Task Force have attempted to do and,
whenever possible or appropriate, steps in management
have also been suggested. This document is not intended
to be all-inclusive or to substitute for textbooks on
paediatric and neonatal ECG.
The manuscript has been reviewed by the Members of
the CPGPC: Werner Klein (Chair), Maria Angeles Alonso,
Gianfranco Mazzotta, Carina Blomstrom Lundqvist. The authors
are grateful to Pinuccia De Tomasi, BS, for expert editorial support
in the preparation of the manuscript.
References
[1] Schwartz PJ, Stramba-Badiale M, Segantini A et al. Prolongation of the QT interval and the sudden infant death
syndrome. N Engl J Med 1998; 338: 170914.
[2] Schwartz PJ, Priori SG, Bloise R et al. Molecular diagnosis in
a child with sudden infant death syndrome. Lancet 2001; 358:
13423.
[3] Davignon A, Rautaharju P, Boisselle E, Soumis F, Megelas
M, Choquette A. Normal ECG standards for infants and
children. Pediatr Cardiol 1979; 1: 12352.
[4] Rijnbeek PR, Witsenburg M, Schrama E, Hess J, Kors JA.
New normal limits for the paediatric electrocardiogram. Eur
Heart J 2001; 22: 70211.
[5] Garson A Jr. Electrocardiography. In: Garson A Jr, Bricker
JT, Fisher DJ, Neish SR, eds. The Science and Practice of
Paediatric Cardiology, 2nd edn. Baltimore, MD: Williams &
Wilkins, 1998: 71388.
[6] Tippel M. Interpretation of electrocardiograms in infants
and children. Images Paediatr Cardiol 1999; 1: 313 available
at:
http://www.health.gov.mt/impaedcard/issue/issue1/ecg1/
ect1.htm#top
[7] Garson A Jr. Clinically significant dierences between the
old analog and the new digital electrocardiograms. Am
Heart J 1987; 114 (1 Pt 1): 1947.
[8] Rijnbeek PR, Kors JA, Witsenburg M. Minimum bandwidth
requirements for recording of paediatric electrocardiograms.
Circulation 2001; 104: 308790.
[9] Yamamoto H, Miyahara H, Domae A. Is a higher sampling
rate desirable in the computer processing of the paediatric
electrocardiogram? J Electrocardiol 1987; 20: 3218.
[10] Macfarlane PW, Coleman EN, Pomphrey EO, McLaughlin S,
Houston A, Aitchison T. Normal limits of the high-fidelity
paediatric ECG. Preliminary observations. J Electrocardiol
1989; 22 (Suppl): 1628.
[11] Bailey JJ, Berson AS, Garson A Jr et al. Recommendations
for standardization and specifications in automated electrocardiography: bandwidth and digital signal processing. A
report for health professionals by an ad hoc writing group of
the Committee on Electrocardiography and Cardiac Electrophysiology of the Council on Clinical Cardiology, American
Heart Association. Circulation 1990; 81: 7309.
Eur Heart J, Vol. 23, issue 17, September 2002
1344
[12] Stramba-Badiale M, Lazzarotti M, Schwartz PJ. Development of cardiac innervation, ventricular fibrillation, and
sudden infant death syndrome. Am J Physiol 1992; 263:
H151422.
[13] Thomaidis C, Varlamis G, Karamperis S. Comparative study
of the electrocardiograms of healthy fullterm and premature
newborns. Acta Paediatr Scand 1988; 77: 6537.
[14] Stramba-Badiale M, Spagnolo D, Bosi G, Schwartz PJ. Are
gender dierences in QTc present at birth? MISNES Investigators. Multicenter Italian Study on Neonatal Electrocardiography and Sudden Infant Death Syndrome. Am J Cardiol
1995; 75: 12778.
[15] Schwartz PJ, Montemerlo M, Facchini M et al. The QT
interval throughout the first 6 months of life: a prospective
study. Circulation 1982; 66: 496501.
[16] Vincent GM. Heart rate of RomanoWard syndrome
patients. Am Heart J 1986; 112: 614.
[17] Hofbeck M, Ulmer H, Beinder E, Sieber E, Singer H. Prenatal
findings in patients with prolonged QT interval in the neonatal
period. Heart 1997; 77: 198204.
[18] Ho SY, Fagg N, Anderson RH, Cook A, Allan L. Disposition
of the atrioventricular conduction tissues in the heart with
isomerism of the atrial appendages: its relation to congenital
complete heart block. J Am Coll Cardiol 1992; 20: 90410.
[19] Brucato A, Frassi M, Franceschini F et al. Risk of congenital
complete heart block in newborns of mothers with anti-Ro/
SSA antibodies detected by counterimmunoelectrophoresis: a
prospective study of 100 women. Arthritis Rheum 2001; 44:
18325.
[20] Buyon JP, Hiebert R, Copel J et al. Autoimmune-associated
congenital heart block: long-term outcome of children and
immunogenetic study. J Am Coll Cardiol 1998; 31: 165866.
[21] Geggel RL, Tucker L, Szer I. Postnatal progression from
second to third degree heart block in neonatal lupus syndrome. J Pediatr 1988; 113: 104952.
[22] Trippel DL, Parsons MK, Gillette PC. Infants with long-QT
syndrome and 2:1 atrio-ventricular block. Am Heart J 1995;
130: 11304.
[23] Gorgels APM, Al Fadley F, Zaman L, Kantoch MJ, Al
Halees Z. The long QT syndrome with impaired atrioventricular conduction: a malignant variant in infants. J Cardiovasc
Electrophysiol 1998; 9: 122532.
[24] Van Hare GF, Franz MR, Roge C, Scheinman MM. Persistent functional atrio-ventricular block in two patients with
prolonged QT intervals: elucidation of the mechanism of
block. PACE 1990; 13: 60818.
[25] Lupoglazo JM, Cheav T, Baroudi G et al. Homozygous
SCN5A mutation in long QT syndrome with functional
two-to-one atrioventricular block. Circ Res 2001; 89: e16e21.
[26] Villain E, Kachaner J, Le Bidois J et al. Bloc auricoloventriculaire partiel et allongement de QT chez quatre prematures recevant du diphemanil. Arch Fr Pediatr 1990; 47: 335.
[27] Southall DP, Johnson AM, Shinebourne EA, Johnston PG,
Vulliamy DG. Frequency and outcome of disorders of cardiac
rhythm and conduction in a population of newborn infants.
Paediatrics 1981; 68: 5866.
[28] Gnota JF, Samson RA. Left bundle branch block in infants with dilated cardiomyopathy conveys a poor prognosis.
Cardiol Young 1999; 9: 557.
[29] Stephan E, de Meeus A, Bouvagnet P. Hereditary bundle
branch defect: right bundle branch blocks of dierent causes
have dierent morphologic characteristics. Am Heart J 1997;
133: 24956.
[30] Brink PA, Ferreira A, Moolman JC, Weymar HW, van der
Merwe PL, Corfield VA. Gene for progressive familial heart
block type I maps to chromosome 19q13. Circulation 1995;
91: 163340.
[31] Ewing LL. Intraventricular conduction disturbances in children. Prog Pediatr Cardiol 1994; 4: 1119.
[32] Perry JC, Giure RM, Garson A. Clues to the electrocardiographic diagnosis of subtle WolParkinsonWhite syndrome. J Pediatr 1990; 117: 8715.
Eur Heart J, Vol. 23, issue 17, September 2002
[33] Sorbo MD, Buja GF, Miorelli M et al. The prevalence of the
WolParkinsonWhite syndrome in a population of 116 542
young males. G Ital Cardiol 1995; 25: 6817.
[34] Munger TM, Packer DL, Hammill SC et al. A population
study of the natural history of WolParkinsonWhite syndrome in Olomsted County, Minnesota, 19531989. Circulation 1993; 87: 86673.
[35] Paul T, Guccione P, Garson A Jr. Relation of syncope in
young patients with WolParkinsonWhite syndrome to
rapid ventricular response during atrial fibrillation. Am J
Cardiol 1990; 65: 31821.
[36] Deal BJ, Keane JF, Gillette PC, Garson A. WolParkinson
White syndrome and supraventricular tachycardia during
infancy: management and follow-up. J Am Coll Cardiol 1985;
5: 1305.
[37] Perry JC, Garson A. Supraventricular tachycardia due to
WolParkinsonWhite syndrome in children: early disappearance and late recurrence. J Am Coll Cardiol 1990; 16:
121520.
[38] Saul JP, Walsh EP, Triedman JK. Mechanisms and therapy of
complex arrhythmias in paediatric patients. J Cardiovasc
Electrophysiol 1995; 6: 112948.
[39] Villain E, Bonnet D, Acar P, Aggoun Y, Sidi D, Kachaner J.
Recommendations for the treatment of recurrent supraventricular tachycardia in infants. Arch Pediatr 1998; 5:
1338.
[40] Stramba-Badiale M, Nador F, Porta N et al. QT interval
prolongation and risk of life-threatening arrhythmias during
toxoplasmosis prophylaxis with spiramycin in neonates. Am
Heart J 1997; 133: 10811.
[41] Cimaz R, Stramba-Badiale M, Brucato A, Catelli L, Panzeri
P, Meroni PL. QT interval prolongation in asymptomatic
anti-SSA/Ro-positive infants without congenital heart block.
Arthritis Rheum 2000; 43: 104953.
[42] Schwartz PJ, Priori SG, Napolitano C. The long QT syndrome. In: Zipes DP, Jalife J, eds. Cardiac electrophysiology:
from cell to bedside, 3rd edn. Philadelphia: WB Saunders,
2000: 597615.
[43] Priori SG, Napolitano C, Schwartz PJ. Low penetrance in the
long QT syndrome. Clinical impact. Circulation 1999; 99:
52933.
[44] Schwartz PJ, Priori SG, Dumaine R et al. A molecular link
between the sudden infant death syndrome and the long-QT
syndrome. N Engl J Med 2000; 343: 2627.
[45] Ackerman MJ, Siu BL, Sturner WQ et al. Postmortem
molecular analysis of SCN5A defects in sudden infant death
syndrome. JAMA 2001; 286: 22649.
[46] Schwartz PJ, Priori SG, Spazzolini C et al. Genotypephenotype correlation in the long-QT syndrome: gene-specific
triggers for life threatening arrhythmias. Circulation 2001;
103: 8995.
[47] Garson A Jr, Dick M 2nd, Fournier A et al. The long QT
syndrome in children. An international study of 287 patients.
Circulation 1993; 87: 186672.
[48] Malfatto G, Beria G, Sala S, Bonazzi O, Schwartz PJ.
Quantitative analysis of T wave abnormalities and their
prognostic implications in the idiopathic long QT syndrome.
J Am Coll Cardiol 1994; 23: 296301.
[49] Villain E, Levy M, Kachaner J, Garson A Jr. Prolonged QT
interval in neonates: benign, transient, or prolonged risk of
sudden death. Am Heart J 1992; 124: 1947.
[50] Brugada J, Brugada R, Brugada P. Right bundle branch block
and ST-segment elevation in leads V1 through V3: a marker
for sudden death in patients without demonstrable structural
heart disease. Circulation 1998; 97: 45760.
[51] Priori SG, Napolitano C, Giordano U, Collisani G, Memmi
M. Brugada syndrome and sudden cardiac death in children.
Lancet 2000; 355: 8089.
[52] Suzuki H, Torigoe K, Numata O, Yazaki S. Infant case with
a malignant form of Brugada Syndrome. J Cardiovasc
Electrophysiol 2000; 11: 127780.